Retina — Macular disease

AMD: diagnosis and management

Age-related macular degeneration (AMD) is the leading cause of low vision after the age of 50 in France. Diagnosed early and managed promptly when required, its progression can be slowed, and in its exudative form, stabilised by effective treatments. Here is the complete care pathway: OCT screening, OCT-A angiography, intravitreal anti-VEGF injections in a dedicated room.

What is AMD?

AMD — age-related macular degeneration — is a degenerative condition that affects the macula, the central zone of the retina responsible for the precise vision used to read, recognise a face, or drive. It most often affects people over the age of 50 and is the leading cause of visual disability in adults in industrialised countries.

AMD does not cause blindness in the strict sense: peripheral vision is preserved. But the decline in central vision considerably impairs daily independence: reading becomes difficult, recognising faces is compromised, and driving becomes dangerous. Prevalence rises sharply with age: rare before 55, it affects roughly 1 person in 4 beyond the age of 75, across all forms combined.

There are two main clinical forms, often distinct but sometimes combined:

Atrophic (or dry) AMD — the most common (around 80% of cases), characterised by the progressive loss of retinal cells at the level of the macula. Progression is slow, spread over several years.
Exudative (or wet, or neovascular) AMD — less common but far more aggressive. Abnormal new vessels develop beneath the macula, leak fluid and blood, and can cause severe visual loss within a few weeks. This form is a therapeutic emergency: the earlier it is treated, the more favourable the prognosis.

Symptoms: recognising AMD

The symptoms of AMD vary depending on the form and stage. The most common ones to report at the consultation:

Distortion of straight lines (metamorphopsia) — window frames, tiling, and lines of text appear wavy or twisted. This is a major warning sign of early exudative disease.
Central dark spot (scotoma) — a blurred or greyed-out area appears in the centre of the visual field.
Progressive decline in visual acuity, particularly for fine reading.
Need for stronger lighting to read, difficulty adjusting vision when brightness changes.
Altered colours and contrasts, perceived as less vivid than before.

Self-monitoring is made easier by the Amsler grid, which I am happy to provide at the consultation: a simple grid held at 30 cm, one eye at a time, allows early detection of distortion or a central scotoma. Any recent onset of metamorphopsia should prompt a prompt consultation.

Risk factors

Several factors increase the risk of AMD, some modifiable, others not:

Age — the leading factor; prevalence doubles every 10 years beyond the age of 55.
Smoking — this is the most important modifiable factor. Tobacco increases the risk of AMD and of progression to advanced forms by 2 to 4 times. Quitting remains beneficial at any age.
Family history — a well-documented genetic predisposition. An affected first-degree relative doubles the risk.
Diet — a diet low in fruit, green vegetables, and oily fish promotes the disease; conversely, a Mediterranean-style diet slows its progression.
Cumulative sun exposure without UV protection — a debated but plausible factor.
Associated cardiovascular conditions (high blood pressure, high cholesterol) — sharing mechanisms of microvascular damage.
Female sex — slightly more exposed, partly linked to longer life expectancy.

Quitting smoking, a balanced diet rich in antioxidants and omega-3, and appropriate sun protection are the first-line prevention measures, to be put in place at any stage.

Diagnosis: OCT and OCT-A angiography

The diagnosis of AMD relies on a combination of clinical examination and specialised imaging. At the office, the consultation includes a detailed history (medical background, lifestyle, symptoms), a measurement of visual acuity, an Amsler grid test, then a complete fundus examination after pupil dilation.

Macular OCT — the reference examination

Optical coherence tomography (OCT) is today the reference examination for the diagnosis and follow-up of AMD. In a few seconds it produces a cross-sectional image of the macula, much like an optical scanner, without injection and without contact.

Both of my offices are equipped with complementary OCT systems, which allows care tailored to each patient:

Cachan office — Cirrus 6000 (Zeiss) OCT, a reference spectral-domain platform (SD-OCT) used for standard follow-up, measurement of retinal thicknesses, and quantification of drusen in atrophic AMD.
Paris 13 office — Diabet’ — TowardPi YAlkaid (YG-100K) OCT, a latest-generation swept-source platform (SS-OCT) at 1060 nm and 100 kHz, with an integrated ultra-wide-field OCT-A angiography module. This technology is particularly suited to detailed exploration of the choroid and to the detection of new vessels, including type 1 new vessels (sub-retinal pigment epithelium) that are difficult to visualise with conventional SD-OCT.

OCT makes it possible to distinguish atrophic forms (analysis of areas of geographic atrophy, measurement of their progression) from exudative forms (detection of intra- or sub-retinal fluid, identification of a retinal pigment epithelium detachment, search for active new vessels).

OCT-A angiography — visualising new vessels

OCT angiography (OCT-A) is a recent and major evolution of OCT: it maps the retinal and choroidal vessels without injecting any dye (no fluorescein or ICG), by analysing the signal linked to blood flow at each level of depth. The examination is fast, non-invasive, and without side effects.

At the Paris 13 office I have the OCT-A integrated into the TowardPi YAlkaid, with the ability to obtain in a single scan a field of 15×15 mm — significantly wider than conventional OCT-A (usually 6×6 or 12×12 mm). This extended field is particularly useful to:

Identify and precisely locate a suspect new vessel on structural OCT
Explore the choroid, the site of type 1 new vessels (common in exudative AMD)
Follow the evolution of a new vessel under treatment, by measuring changes in the abnormal vascular surface
Map microvascular alterations in atrophic forms, sometimes precursors of conversion to the exudative form

In cases where OCT-A is not sufficient (complex differential diagnosis, atypical retrofoveal new vessels, suspicion of polypoidal vasculopathy), conventional fluorescein or indocyanine green angiography remains indicated, as a complement and in a specialised centre.

Atrophic (dry) AMD — monitoring and prevention

Atrophic AMD progresses slowly, over several years, through the gradual loss of retinal pigment epithelium cells and the overlying photoreceptors. There is currently no curative treatment able to restore the lost cells. Management relies on three complementary approaches:

1. Close follow-up and self-monitoring

The main risk is the conversion of an atrophic form into an exudative form — an event that radically changes management and can occur at any time. For this reason close monitoring is essential: OCT assessments every 6 to 12 months depending on the stage, weekly self-checks with the Amsler grid between consultations, and a prompt consultation if metamorphopsia or a sudden visual decline appears.

2. AREDS2 nutritional supplementation

The American study Age-Related Eye Disease Study 2 (AREDS2, Chew et al., JAMA, 2013) demonstrated that daily supplementation with specific antioxidants and trace elements reduces by about 25% the risk of progression to advanced AMD in patients with an intermediate form. The AREDS2 formulation combines vitamins C and E, zinc, copper, lutein, and zeaxanthin. The omega-3 tested in the study did not show any additional benefit on retinal progression but retain a cardiovascular interest documented elsewhere.

This supplementation is recommended in intermediate AMD (confluent drusen, pigmentary alterations) and in cases where one eye is already affected by an advanced form. It is not useful in isolated early forms, nor to prevent the onset of AMD in an unaffected person.

3. Suitable lifestyle

Quitting smoking — the most impactful measure, with documented benefit even after the age of 70.
Mediterranean diet — green vegetables (natural lutein/zeaxanthin), colourful fruit, oily fish, olive oil.
Sun protection — UV-filtering glasses during prolonged exposure, particularly at the sea or in the mountains.
Control of cardiovascular factors — high blood pressure, diabetes, and cholesterol kept balanced together with your general practitioner.

Exudative (wet) AMD — intravitreal anti-VEGF injections

Exudative AMD is characterised by the development of abnormal new vessels beneath the macula, which leak fluid and blood. Without treatment, the disease can lead within a few months to a definitive central fibrous scar, with major loss of central vision. Modern treatment relies on intravitreal anti-VEGF injections — molecules that block the signal stimulating the formation of new vessels.

This treatment has transformed the prognosis of the disease: today, the majority of patients treated early maintain or improve their visual acuity, whereas twenty years ago they almost systematically lost their central vision. The earliness of treatment determines the outcome: every week of delay counts.

The anti-VEGF agents used in practice

The anti-VEGF agents I use at the office for exudative AMD include aflibercept (Eylea and high-dose Eylea HD), faricimab (Vabysmo), and ranibizumab (Lucentis). The choice and the therapeutic sequence are tailored to each patient’s profile: response to injections, time to recurrence of activity, ease of follow-up, and tolerance.

Aflibercept 8 mg (Eylea HD) — a high-dose formulation of aflibercept, approved in Europe in 2024. Its pharmacokinetic profile makes it possible, in a significant proportion of cases, to space injections out to 12 to 16 weeks after the 3 initial monthly injections. The phase 3 PULSAR study (Lanzetta et al., Lancet, 2024) demonstrated the non-inferiority of aflibercept 8 mg compared with conventional aflibercept 2 mg every 8 weeks, with a benefit in terms of spacing out visits.
Faricimab (Vabysmo) — a bispecific antibody that simultaneously inhibits VEGF-A and angiopoietin-2, two complementary pathways involved in neoangiogenesis and vascular permeability. The TENAYA and LUCERNE studies (Heier et al., Lancet, 2022) showed that faricimab makes it possible, in a proportion of patients, to extend injection intervals out to 16 weeks with a visual outcome comparable to aflibercept 2 mg every 8 weeks.
Ranibizumab (Lucentis) — the pioneering anti-VEGF-A in the management of exudative AMD, still used in certain indications depending on the patient’s profile and updated recommendations.

Bevacizumab (Avastin), used off-label in some hospital centres, is not included in my private-practice protocol.

Treatment schedule: induction phase then treat-and-extend

Treatment begins with an induction phase of 3 monthly injections, intended to rapidly dry out the active new vessels. Beyond that, the strategy followed is treat-and-extend (T&E): the interval between two injections is adjusted according to the activity observed on the OCT at each check-up. When the retina is dry, the interval is gradually extended; in the event of recurrence, it is brought closer. The aim is to maintain a fluid-free retina with the fewest possible injections, to preserve vision and limit the treatment burden.

In practice, a typical patient on a recent anti-VEGF agent may receive 6 to 8 injections in the first year, with a tendency towards a gradual reduction in the number of injections needed over time, as the neovascular activity stabilises.

Performing the injections in a dedicated room

I perform intravitreal injections in a dedicated room in Cachan and in Paris 13, in line with the recommendations of the French Society of Ophthalmology and the HAS: strict aseptic conditions, skin and conjunctival disinfection with povidone iodine, topical anaesthesia, and injection through the pars plana under sterile conditions. The procedure takes a few minutes, the pain is very mild, and the patient leaves immediately after a brief check.

The rare but important side effects to be aware of include a foreign-body sensation for 24 to 48 hours, small subconjunctival haemorrhages of no consequence, and, exceptionally, a risk of endophthalmitis (intraocular infection), the rate of which under modern conditions is in the order of 1 per 3,000 to 5,000 injections. A strict instruction is given to every patient: seek emergency care in the event of unusual eye pain, sudden visual decline, or marked redness in the days following the injection.

Photodynamic therapy (PDT) — referral if necessary

In certain particular forms of exudative AMD — notably polypoidal choroidal vasculopathy, a subtype that sometimes responds incompletely to anti-VEGF agents alone — photodynamic therapy with verteporfin (PDT) may be combined with treatment. I do not perform PDT, and in these cases I refer to a specialised centre, while maintaining follow-up in close coordination.

Dr Tourabaly’s view

“AMD remains an anxiety-inducing condition for patients, who fear blindness. My role is to place the disease back in its reality: peripheral vision is always preserved, the atrophic form progresses slowly over years, and the exudative form can today be stabilised in the vast majority of cases when it is managed early. Having an OCT and an OCT angiography in both offices, and performing the injections in a dedicated room on site, allows a smoothness of the care pathway that makes a real difference to the long-term outcome.”

Patient care pathway

Cachan office (94) — consultations, Cirrus 6000 OCT, intravitreal injections in a dedicated room. Telephone: 01 45 47 08 11.
Paris 13 office — Diabet’ — consultations, TowardPi YAlkaid swept-source OCT with ultra-wide-field OCT-A, intravitreal injections in a dedicated room. Telephone: 01 89 31 30 60.

Consultation appointments can be booked directly on Doctolib. A recent onset of metamorphopsia or a central scotoma should be the subject of a prompt consultation, without waiting for the usual scheduled appointment.

Frequently asked questions

Yes, the recent onset of metamorphopsia (lines that wave or distort) is a warning sign of early exudative AMD. A prompt consultation is recommended to perform an OCT and, if needed, start treatment without delay. The earlier the management, the more favourable the long-term visual outcome.

The number of injections depends on each patient’s profile and the molecule used. Schematically: 3 initial monthly injections, then a rhythm adapted to the progression, often 4 to 6 additional injections in the first year on average. The recent molecules (Eylea HD, Vabysmo) allow, in some patients, spacing out to 12 or 16 weeks, which reduces the total number of annual injections.

The sensation of pain is very mild thanks to topical anaesthesia. Most patients describe a brief discomfort, a short pressure, less intense than anticipated. In the following 24 to 48 hours, a slight foreign-body sensation or a reddened eye (subconjunctival haemorrhage of no consequence) is possible but fades spontaneously. Significant pain, a visual decline, or marked redness in the following days should, however, prompt an emergency consultation.

Not systematically, but the risk is significantly increased. Epidemiological studies show that around one patient in two with advanced AMD in one eye will develop involvement of the other eye within five years. For this reason, monitoring of the fellow eye is rigorous, and self-checking with the Amsler grid, one eye at a time, is systematically taught.

Yes, in intermediate forms. The AREDS2 study demonstrated that specific supplementation (vitamins C and E, zinc, copper, lutein, zeaxanthin) reduces by about 25% the risk of progression to advanced AMD in the patients concerned. A Mediterranean diet rich in green vegetables, colourful fruit, and oily fish naturally provides some of these nutrients. Quitting smoking remains the most effective measure, at any stage.

Book an appointment for an AMD assessment

Appointment in Cachan

Appointment in Paris 13

Sources

Age-Related Eye Disease Study 2 (AREDS2) Research Group, Chew EY, Clemons TE, et al. Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. JAMA. 2013;309(19):2005-2015. PMID: 23644932
Heier JS, Khanani AM, Quezada Ruiz C, et al. Efficacy, durability, and safety of intravitreal faricimab up to every 16 weeks for neovascular age-related macular degeneration (TENAYA and LUCERNE): two randomised, double-masked, phase 3, non-inferiority trials. Lancet. 2022;399(10326):729-740. PMID: 35085502
Lanzetta P, Korobelnik JF, Heier JS, et al. Intravitreal aflibercept 8 mg in neovascular age-related macular degeneration (PULSAR): 48-week results from a randomised, double-masked, non-inferiority, phase 3 trial. Lancet. 2024;403(10432):1141-1152. PMID: 38461841

This article is for informational purposes. A personalised ophthalmological opinion remains essential for any therapeutic decision.

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